Abstract: Background and purpose: Selenium is one of the essential trace elements for human activities, and plays an incomparable role in maintaining human health. It was reported that selenium compound 1,4-bis［2-(benzylselanyl) ethoxy］ (BSEA) anthracene has antiseptic and antiphlogistic effects. However, the mechanisms underlying anticancer effects of BSEA are rarely reported. BSEA-induced apoptosis in human laryngeal carcinoma Hep-2 cells and its mechanisms were studied. Methods: Methyl thiazolyl tetrazolium (MTT) assay was used to determine inhibition ratio of Hep-2 cells 24 hours after Hep-2 cells were treated with different concentrations of BSEA. Fluorescence microscope was used to observe the morphology change of apoptosis in Hep-2 cells. The apoptosis was detected by Annexin Ⅴ-FITC. Mitochondrial membrane potential was assayed by JC-1. Microplate reader detected the activity of caspase-3 and caspase-8. The mRNA and protein levels of Bax and XIAP were measured by real-time fluorescent quantitative polymerase chain reaction (RTFQ-PCR) and Western blot. Results: The results showed that BSEA caused a dose-dependent inhibition of the growth of human laryngeal carcinoma cell line Hep-2 in vitro, and IC50 was 35.74 μmol/L. The apoptotic bodies were distinctly observed at a concentration of 80 μmol/L of BSEA by AO fluorescence staining. This study found that the eversion of phosphatidyl serine intensified, and mitochondrial membrane potential also began to decline. The activity of caspase-3 appeared the tendency of dependence on dosage, while the activity of caspase-8 did not change significantly. The mRNA and protein expression level of Bax increased, whereas the mRNA and protein expression level of XIAP decreased. Conclusion: Therefore, BSEA could obviously inhibit human laryngeal carcinoma Hep-2 cells proliferation and induce apoptosis via the mitochondrial pathway.

Key words: 1,4-bis［2-(benzylselanyl)ethoxy］ anthracene, Hep-2 cells, Apoptosis, Mitochondrial pathway